Melatonin ameliorated okadaic-acid induced Alzheimer-like lesions

Yi Peng Wang, Xian Tao Li, Shi Jie Liu, Xin Wen Zhou, Xiao Chuan Wang, Jian Zhi Wang

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30 Citations (Scopus)


AIM: To explore the protective effects of melatonin (Mel) on the abnormal phosphorylation of neuronal cytoskeletal proteins. METHODS: We generated a neuroblastoma (SH-SY5Y) cell system in which cytoskeletal proteins are abnormally phosphorylated resulting in microtubule disruption due to the marked inhibition of protein phosphatase activities by okadaic acid (OA). RESULTS: OA-induced declines in cell viability and mitochondrial metabolic activity were remarkably prevented by Mel. In addition, the hyperphosphorylation/accumulation of neurofilament-(NF-) H/M subunits and the disruption of microtubules, induced by OA, were significantly inhibited by Mel. CONCLUSION: Our results suggest multiple protective functions of Mel against a series of pathological lesions known to culminate in AD, including abnormal phosphorylation of cytoskeletal proteins, microtubule disassembly and mitochondrion-initiated cell toxicity.

Original languageEnglish
Pages (from-to)276-280
Number of pages5
JournalActa Pharmacologica Sinica
Issue number3
Publication statusPublished - 1 Mar 2004
Externally publishedYes


  • Alzheimer disease
  • Melatonin
  • Neurofilament proteins
  • Okadaic acid
  • Protein phosphatase

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